Stimulant use disorder (cocaine, amphetamines) !

Hard-to-control use of cocaine, basuco or amphetamines that causes harm. Intoxication can cause heart attack, stroke and psychosis; withdrawal brings a crash.

Updated 2026-11-01

Structures involved

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Why it happens

What it is

A substance use disorder involving cocaine (powder, crack or coca paste such as basuco) or amphetamine-type stimulants (methamphetamine, amphetamine, MDMA), in which repeated use leads to loss of control, craving and harm. This page also covers the acute effects of intoxication and the withdrawal syndrome, which students are commonly examined on.

Who gets it

Colombia is a major cocaine producer and, along with other Latin American countries, has rising domestic use of cocaine and basuco, especially among young men and people living on the street. Amphetamine-type stimulants and synthetic drugs (such as tusi, a mixture sold as pink cocaine) are growing among young adults in cities. Cocaine is a leading drug-related cause of emergency visits for chest pain.

Causes

Repeated use of a drug that strongly increases brain dopamine, reinforcing the behaviour
Genetic vulnerability and family history of addiction
Early first use in adolescence, peer and environmental exposure
Coexisting mental disorders (ADHD, depression, PTSD) and use of other substances, especially alcohol

Risk factors

Male sex and age 18 to 35
Easy drug availability and poverty, homelessness or displacement
Childhood adversity and trauma
Use of alcohol or tobacco from an early age
Smoked or injected routes, which act faster and are more addictive

Pathophysiology

Cocaine blocks reuptake of dopamine, noradrenaline and serotonin; amphetamines also release these transmitters from the nerve endings. The sudden rise in dopamine in the mesolimbic reward pathway (ventral tegmental area to the ventral striatum) produces euphoria and reinforces use; prefrontal control weakens over time. Excess noradrenaline causes vasoconstriction, tachycardia and hypertension, with coronary spasm and increased platelet aggregation. After a binge, depleted dopamine produces the 'crash'.

Classification

Severity by number of DSM-5 criteria: mild (2–3), moderate (4–5), severe (6 or more)
By substance: cocaine-type or amphetamine-type
Intoxication: euphoria, hyperactivity, dilated pupils, tachycardia, hypertension, hyperthermia, possible psychosis
Withdrawal: dysphoria, fatigue, hypersomnia, increased appetite, vivid dreams and intense craving

Symptoms and signs

Intoxication: euphoria, talkativeness, agitation, little need for sleep and grandiosity
Dilated pupils, sweating, tachycardia, hypertension and fever
Paranoia, hallucinations (for example tactile 'bugs' under the skin, formication) and violent behaviour
Chest pain, palpitations or seizures during use
Withdrawal crash: deep sadness, exhaustion, long sleep, hunger and craving; suicidal ideation is possible
Chronic signs: weight loss, nasal septum perforation from snorting, dental damage with methamphetamine, burns on lips or fingers from smoking

Diagnosis

Clinical: History of use and DSM-5 criteria (loss of control, craving, failure of roles, tolerance, withdrawal, continuing despite harm). In intoxication, a sympathomimetic toxidrome: tachycardia, hypertension, hyperthermia, mydriasis and sweating (unlike anticholinergic toxicity, the skin is wet).
Tests: Urine drug screen (cocaine metabolite benzoylecgonine positive for about 2–4 days; amphetamines 1–3 days). ECG and troponin for chest pain; creatine kinase, kidney function and electrolytes for rhabdomyolysis; glucose; screening for HIV, hepatitis B and C and syphilis in people who inject or exchange sex.
Imaging: Chest X-ray or CT angiography if aortic dissection is suspected; head CT for seizures, severe headache or focal signs; abdominal imaging in suspected body packing.

Differential diagnosis

Anticholinergic toxicity (dry skin, urinary retention)
Serotonin syndrome or neuroleptic malignant syndrome
Thyrotoxicosis or pheochromocytoma
Alcohol or sedative withdrawal
Primary psychotic disorder or mania in bipolar disorder

Goal of treatment

Stabilise acute intoxication and its complications, then achieve abstinence or reduced use, treat coexisting disorders and reduce harm.

Treatment

Acute: Intoxication: benzodiazepines are first line for agitation, tachycardia, hypertension and seizures; active cooling for hyperthermia; avoid pure beta-blockers in acute cocaine toxicity (concern for unopposed alpha stimulation)
Acute: Cocaine chest pain: benzodiazepines, aspirin, nitrates and, if needed, a calcium-channel blocker or phentolamine; standard treatment of myocardial infarction
Conservative: Contingency management (rewards for negative urine tests), the most effective treatment for stimulant use disorder
Conservative: Cognitive behavioural therapy, motivational interviewing and community or residential programmes
Medical: No medication is approved for stimulant use disorder; treat coexisting depression, ADHD or psychosis with appropriate classes
Follow-up: Nursing: monitor vital signs and temperature, quiet safe environment, suicide risk during withdrawal, harm-reduction counselling

Complications

Myocardial infarction, arrhythmias, cardiomyopathy and aortic dissection
Ischaemic stroke and intracerebral haemorrhage; seizures
Hyperthermia, rhabdomyolysis and acute kidney injury
Stimulant-induced psychosis, depression and suicide
HIV, hepatitis B and C infection; nasal septum perforation; levamisole-adulterant vasculitis and neutropenia

Prognosis

Relapse is frequent, but many people achieve long-term remission with psychosocial treatment. Smoked forms (crack, basuco) and methamphetamine carry worse outcomes. Sudden death can occur even in first-time users from arrhythmia or stroke.

Prevention

Prevention programmes in schools and communities
Early treatment of ADHD and depression
Harm-reduction services and public-health policies that reduce availability and stigma

Test yourself

Think of the answer, then tap the question to see it.

A 28-year-old man has chest pain after snorting cocaine. What is the first-line drug class for agitation and hypertension?

Benzodiazepines.

Which drug class is classically avoided in acute cocaine toxicity?

Non-selective beta-blockers, because of unopposed alpha-adrenergic vasoconstriction.

What are the typical features of stimulant withdrawal?

Dysphoria, fatigue, hypersomnia, increased appetite and craving (with risk of suicidal ideation).

What is the most effective treatment for stimulant use disorder?

Contingency management combined with behavioural therapy; no medication is approved.

How does the sympathomimetic toxidrome differ from the anticholinergic one?

In sympathomimetic toxicity the skin is sweaty and bowel sounds are present; anticholinergic toxicity causes dry skin and urinary retention.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Cocaine (National Institute on Drug Abuse (NIDA), 2025); Methamphetamine (National Institute on Drug Abuse (NIDA), 2025); Cocaine intoxication (MedlinePlus (U.S. National Library of Medicine), 2025).

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Representative model, for educational purposes only.

Frontal lobe highlighted on the Durgical 3D model